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Excerpt
Patients with Crohn disease often complain of diarrhea and abdominal pain. These symptoms may be caused in part to altered intestinal motility. Acute ileitis induces significant alterations in smooth muscle contractility that may reflect changes in excitatory and/or inhibitory neurotransmission.Aim: To compare the neural control of smooth muscle contractility in acute ileitis. Methods: Male, Sprague-Dawley rats (n=5-8) were injected with saline (CONTROL) or TNBS (100 mg/kg, ILEITIS) 10 cm proximal to the ileocecal junction. The distal ileum was removed after 4 hrs. Mucosa-free segments were mounted in organ baths in their circular axis and stretched to Lo. Concentration response curves to acetylcholine (ACH), substance P(SP) and neurokinin A (NKA) were constructed. Atropine (ATR, 1μM), hexamethonium (HEX, 10 μM) or a nonselective (L-NNA, 10 μM) or inducible(aminoguanidine, AG, 10 μM) NOS inhibitor were used to evaluate cholinergic, nicotinic and nitrergic control. Results: Responses to ACH were not altered by inflammation. Responses to SP were increased in ILEITIS while those to NKA were unchanged. Responses to SP and NKA were unchanged by L-NNA in either groups. In contrast, AG and HEX blunted the response to SP in ILEITIS (12159±1036 vs 9059±1313) only. Responses to SP and NKA were decreased by ATR in ILEITIS. In contrast, ATR increased the response to SP in CONTROL.Table
Conclusions: Inflamed intestinal muscle demonstrated enhanced contractile responses to SP but not to NKA or ACH. The SP responses in ILEITIS were dependent on intact nicotinic and muscarinic pathways. In ILEITIS, the blunted SP response in the presence of AG but not L-NNA supports a role for iNOS released by resident macrophages. Inflamed terminal ileum exhibits abnormal neural control of smooth muscle responses.
